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- W2936558111 abstract "Graft versus host disease (GvHD) occurs in 40% of cases with patients having a MHC I matched bone marrow transplantation (BMT). Mechanisms causing this disease remain to be studied. Here we used a CD8+ T cell transgenic mouse strain (P14/CD45.1+) and DEE mice bearing the foreign antigen (LCMV-GP33-41) to study mechanisms of tolerance in donor derived host specific CD8+ T cells after BMT. We found that host reactive CD8+ T cells were not negatively selected in the thymus and developed comparably to host non-specific CD8+ T cells. Host specific CD8+ T cells ignored the antigen expressed ubiquitously by host cells but they could be activated ex vivo via LCMV (lymphocytic choriomeningitis virus)-infection. Lipopolysaccharides (LPS) induced transient cell damage in DEE mice bearing host specific CD8+ T cells, suggesting that induction of host inflammatory response could break this ignorance. In conclusion, we found that after BMT host specific CD8+ T cells ignore antigen in recipients and that they are only deleted when host antigen is present in the hematopoietic system. Moreover, LPS-induced immune activation contributes to induction of alloreactivity of host specific CD8+ T cells after BMT. Unexpected transmissions of viral pathogens during solid organ transplantation (SOT) can result in severe, life-threatening diseases in transplant recipients. Immune activation contributes to disease onset; however mechanisms balancing the immune response against transmitted virus infection through organ transplantation remain unknown. Here, we found, using LCMV, that transplantation of LCMV infected hearts led to exhaustion of virus specific CD8+ T cells, viral persistence in organs and survival of graft and recipient. Genetic depletion of IL-10 resulted in a strong immune activation, graft dysfunction and death of mice, suggesting that IL-10 was a major regulator of CD8+ T cell exhaustion during SOT. In the presence of memory CD8+ T cells, virus could be controlled; however sufficient antiviral immune response resulted in rejection of transplanted heart. In conclusion, we found that virus transmitted by SOT cannot be controlled by naive recipients due to IL-10 mediated CD8+ T cell exhaustion which thereby prevented immunopathology and graft failure whereas memory mice recipients were able to control the virus and induced graft failure." @default.
- W2936558111 created "2019-04-25" @default.
- W2936558111 creator A5012835015 @default.
- W2936558111 date "2017-02-09" @default.
- W2936558111 modified "2023-09-23" @default.
- W2936558111 title "Role of viral infection in transplantation medicine" @default.
- W2936558111 hasPublicationYear "2017" @default.
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